Review Articles

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http://hdl.handle.net/2003/25616

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J. G. Hengstler
Leibniz Research Centre for Working Environment and Human Factors
Ardeystr. 67
D-44139 Dortmund
Germany

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L. S. Weilemann, Mainz, Germany
I. Ishibashi, Tokyo, Japan
P. Micke, Uppsala, Sweden
J. Timmer, Freiburg, Germany
A. Winterpacht, Erlangen, Germany
B. C. Behera, Pune, India

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ISSN 1611-2156

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Cigarette Smoking and Parkinson's Disease
(2007-10-04) Das, Salil K.; Miller, Leah R.
This is a review on cigarette smoking and Parkinson's disease (PD). The relationship between cigarette smoking and Parkinson's disease is very controversial. Cigarette smoking is an established risk factor for various diseases such as lung cancer, COPD and heart disease. However, beneficial effects have been debated over the years. It was in the late 1950 s that studies reported a negative association between smoking and Parkinson's disease. More recently, several epidemiological studies have found a significant negative association between cigarette smoking and PD. That is, patients who smoke are 50% less likely to have PD when compared to their non-smoker counterparts. This suggests that cigarette smoking may have a "neuroprotective" effect on PD.
Molecular Regulation of Inflammatory Pain and Hyperalgesia - Is NF-?B the Lynchpin?
(2007-03-26) Haddad, John J.
Inflammatory cells and inflammatory mediators are crucially involved in the genesis, persistence and severity of pain following trauma, infection or nerve injury. The mechanisms and pathways mediating pain and nociception are transcriptionally regulated. The transcriptional mediator nuclear factor (NF)-kB plays a major role in regulating the inflammatory milieu, ostensibly via the control of gene expression/suppression. An association has recently emerged to establish a possible link between NF-kB and pain/nociception, purportedly through the regulation of the inflammatory loop and the secretion (biosynthesis) of pro-inflammatory mediators. Current concepts conspicuously indicate that the effective inhibition of this transcription factor and associated upstream kinase(s) and the pathways that regulate its nuclear translocation could be major targets in a new strategy for the alleviation of inflammation and inflammatory-related pain. To better understand this relationship between NF-kB and the evolution of pain and hyperalgesia/nociception, it is imperative to unravel the molecular basis of this process. This survey definitively integrates current themes pertaining to the pivotal role that NF-kB shares in regulating pain through the decoding of implicated molecular pathways and signaling mechanisms.
The Emphatic Role of Mitogen-Activated Protein Kinases (MAPKs) in the Cellular Mechanisms Mediating Alzheimer's Disease
(2007-03-05) Haddad, John J.
Alzheimer's disease (AD) is a neurogenetic condition that affects the processes via which the brain functions. Major observable hallmarks of AD are accumulated clusters of proteins in the brain. These clusters, termed neurofibrillary tangles (NFT), resemble pairs of threads wound around each other in a helix fashion accumulating within neurons. These tangles consist of a protein called Tau, which binds to tubulin, thus forming microtubules. Unlike NFTs, deposits of amyloid precursor protein (ß-APP) gather in the spaces between nerve cells. The nearby neurons often look swollen and deformed, and the clusters of protein are usually accompanied by reactive inflammatory cells, microglia, which are part of the brain's immune system responsible for degrading and removing damaged neurons or plaques. Since phosphorylation/dephosphorylation mechanisms are crucial in the regulation of Tau and ß-APP, a superfamily of mitogen-activated protein kinases (MAPKs) has recently emerged as key regulators of the formation of plagues, eventually leading to dementia and AD. The complex molecular interactions between MAPKs and proteins (plagues) associated with the evolution of AD form a cornerstone in the knowledge of a still burgeoning field of neurodegenerative diseases and ageing. This review overviews current understanding of the molecular pathways related to MAPKs and their role in the development of AD and, possibly, dementia. MAPKs, therefore, may constitute a neurogenetic, therapeutic target for the diagnosis and evolution of a preventative medical strategy for early detection, and likely treatment, of Alzheimer's.

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